Abstract

An ectopic pregnancy is one in which the embryo is implanted outside the uterine cavity. The incidence of such pregnancy has markedly increased in the past decade. This may be a reflection of prompt diagnosis due to easy availability of non-invasive diagnostic tools such as ultrasonography. However, literatures on histarchitectural changes of early ectopic pregnancy are rather scarce and therefore, the present study was conducted on 20 patients of ectopic pregnancy. The various parameters included in this study were location of ectopic pregnancy, side of corpus luteum and histological features of ectopic pregnancy. It was found that the corpus luteum was noticed on the contra lateral side in 5 cases (25%). The trophoblast invasion was predominantly intralumial. Intratubal hemorrhage was generally proportionate to trophoblastic spread which leads to marked destruction of tubal wall. It was concluded that only early diagnosis and treatment before rupture still remains the best management of ectopic pregnancy.

Keywords

Ectopic pregnancy, Trophoblast, Corpus luteum, Histoarchiteucture.

Introduction

In an ectopic pregnancy the embryonic implantation occurs
outside the uterus most commonly in the fallopian
tube. An ectopic pregnancy is a medical emergency, if not
treated in time can lead to fatal consequences. In normal
pregnancy, the fertilized ovum enters the uterus through
fallopian tube in uterine cavity and settles into the uterine
mucosa where it has plenty of room for its growth and
development. About 1% of all pregnancies are noticed in
an ectopic location with implantation not occurring inside
of the uterus. Of these ectopic pregnancies 98% occur in
the fallopian tube. The incidence of ectopic pregnancy has
markedly increased in the past decade [1]. The implanted
ectopic embryo burrows actively into the tubal lining and
its vessels which is responsible for bleeding. The pain
perceived is believed to be caused by prostaglandin released
at the implantation site and also by the free blood
in the peritoneal cavity acting as local irritant. Despite
many notable successes in field of diagnosis of the ectopic
pregnancy, it remains the source of serious maternal
morbidity and mortality.

Material and Methods

A study was conducted on 20 patients of age ranging between
28 to 40 years and having ectopic pregnancy of 2-3
months of gestation. In addition to its presence, the location
of corpus luteum was also noted. The excised part of tissue was taken and fixed in 10% formalin solution and
processed for light microscopy. Each block was serially
sectioned at 6 micron. .Every tenth section was mounted
for histological study and stained with haematoxylene and
eosin and observed under light microscope.

Observations

The ectopic pregnancy was found on left side in 9 cases
and on right side in 11, but the corpus luteum was found
in all cases by inspection. Nineteen pregnancies were in
ampulla and one in infundibulum. The lumen was found
to be tortuous in eleven cases as compared to tubal lumen
in control tube removed in other benign surgical cases.
All tubes showed evidence of trophoblastic proliferation
invading maternal tissues resulting in extravassation of
significant amount of maternal blood. The orientation of
implantation with reference to major blood vessel appeared
to be random. On microscopic examination of
slides, the predominant pattern of spread of the trophoblast
and the hemorrhage could be classified as predominantly
intraluminal, predominantly extraluminal or
combined. The maternal blood vessels were invaded by
trophoblast soon after initial implantation. In predominantly
intraluminal trophoblastic proliferation (Fig, 1C)
the pattern of spread of trophoblast and pattern of the
hemorrhage in majority of cases was proportionate to
each other. In majority of cases the tube was not ruptured
and the blood often leaked out of abdominal ostium of the fallopian tube after filling the lumen. The tubal enlargement
was due to blood clot rather than from conceptual
mass. In these cases three types of endosalpinx were observed.
However, sometimes the entire tubal epithelial
lining was intact. In other cases the tubal epithelium was
either eroded by invading trophoblast or remained as discontinuous
islands located circumferentially along the
periphery of dilated tubal lumen. Luminal dilatation was
caused by the presence of the gestational sac with or
without embryo, by varying amount of trophblastic tissue
but primarily by maternal blood causing destruction and
disruption of fallopian tube. The predominantly exatraluminal
trophoblastic proliferation (Fig, 1D) was found in
minority of cases. But in majority of cases it was associated
with rupture of fallopian tube. The trophoblastic tissue
was proliferated in sheets, between the tissue layers.
The accompanying hemorrhage dissected the tissue layers
and compressed the tubal lumen. In cases of spread of the
combined pattern, spread of the trophoblastic infiltration
and hemorrhage were found both intra luminal as well as
extra luminal sites.

The endosalpinx was well preserved every where except
at the place where initial implantation took place and lead
to breach in the epithelium. In this area the trophoblast
eroded the entire endosalpinx but a portion of the epithelium
was normal in majority of cases. Dilatation of the mucosal lymphatics, stromal edema and lymphocytic infiltration
of the lamina propria were common near the
implantation site (Fig. 1B). Changes in the myosalpinx
appeared to depend upon the stage of pregnancy and
wheather or not predominant trophoblastic growth proceeded
to intraluminal or extraluminal sites. Where luminal
distension was less marked, swelling and edema of
the myosalpinx were commonly seen as marked circumferential
lymphatics distention. When hemorrhages occurred
into myosalpinx blood filled spaces were also visible.
When luminal distension was marked the myosalpinx
became stressed and compressed. Trophblastic invasion
into the myosalpinx ranged from localized penetration by
anchoring villi to complete destruction of muscularis. In
majority of cases trophoblastic invasion was limited to
luminal aspect of the myosalpinx along with inflammatory
cell infiltration. The serosa and subserosa overlying
the site of ectopic pregnancy was usually thinned out so
much so that it became only single layer of mesothelial
cell closely applied to a thin layer of underlying connective
tissue which in turn interfaced with the product of
pregnancy. The mesothelial swelling was common along
with lympocyte infiltration of both serosa and subserosa.
In cases of rupture (Fig. 1D) the serosa was breached by
the invading trophoblast which eroded through the tubal
tissue. In many cases, the invading trophoblast invaded
subserosal blood vessel

Discussion

The present study provided opportunity to extend some
valuable information regarding tubal pregnancy, its mode of occurrence and mechanism of invasion and infiltration
of the tubal wall. It is believed that mechanism of implantation
is that the ovum is picked up by the fimbriated end
of fallopian tube which is held in close contact with ovary by the fimbria ovarica which sweeps across the surface of
ovary during ovulation. The ovum is picked up in its ciliated
fimbria and conducted into the infudibulum of the
tube. In addition to this the ovum pickup can also occur
from pouch of Douglas but the later mechanism is infrequent
because under normal circumstances the ovum
pickup is direct from the ovarian surface to the ipsilateral
tube. When normal human fallopian tube is flushed during
the first three post ovulatory days to recover oocytes,
the search for oocytes is successful in 65% of cases. More
than 95% of recovered oocytes are found in the tube ipsilateral
to the corpus luteum [2]. But in those cases where
the corpus luteum is found on contra lateral side [1] it has
been speculated that some time ovum pick up by fimbria
fails and thus ovum is released into pouch of Douglas.
Possibly a delayed ovum pickup allows fertilization
which leads to advance preimplantation development so
that an expanded blastocyst finds difficulty in crossing the
isthmus and lodged in the ampulla. The other possible
mechanism suggested is that ectopic pregnancy may be
due to dysfunction of ovum transport, the ovum is returned
to the peritoneal cavity by retrograde transport [1].
Ectopic pregnancy is due to delayed ovulation and fertilization,
which fails to suppress menstruation leading to
flushing of fertilized oocyte from uterus to any one of the
fallopian tube due to uterine contraction [3,4]. This increases
the chances of entry of the fertilized ovum into the
opposite tube. Thus, if tubal pregnancy develops it may
be found on the opposite side of corpus luteum. Because
of this fact it is important to establish the relationship of corpus luteum with laterality of the ectopic pregnancy.
These relationship related to menstrual regurgitation are
important because it explain the larger fetus than would
be predicted from menstrual date [5] has suggested that
fallopian cilia is seen to be reduced following ectopic
pregnancy, leading to a hypothesis that cilia damage in
the fallopian tube is likely to lead to an ectopic pregnancy.
Some researchers [6] has concluded that tubal ectopic
pregnancy is caused by a combination of retention
of the embryo within the fallopian tube due to impaired
embryo–tubal transport and alteration in the tubal environment
allowing early implantation to occur.

The ectopic pregnancy induced changes in the histology
of fallopian tube have not been extensively studied. Conservative
management is not specifically taken has effect
of anatomic changes in the histology of tubal pregnancy
and its effect on future of fertility of the patient. As far as
the management is concerned it varies from patient to
patient and it depends upon the age of gestation, site and
time of presentation after rupture of ectopic pregnancy.
Fimbrial evacuation of tubal pregnancy is easy to perform
but it has a high chance of recurrence rate; otherwise if
the gestation sac is large or extra luminal it can not be
evacuated through the lumen and forcible evacuation has
met with increased destruction and further hemorrhage. In this situation first try linear salpingectomy and if tubal
destruction is large and old case of rupture, segmental
resection of the affected tube is better management. Significant
incidence of blighted ovum (anembryonic pregnancy)
has been observed in the tubal pregnancy but its
association with the rupture of the tube with presence or
absence of embryo has not been confirmed [7]. If the observations
concerning the effects of the trophoblast and
the hemorrhage on tubal morphology are confirmed, then
segmental resection becomes the method of choice in reparative
surgery for ectopic pregnancy. In the past salpingectomy
was treatment of choice for management of tubal
pregnancy. Now the current emphasis is on preserving the
reproductive function along with advancement in tubal
surgery and early diagnosis has shifted the attention toward
conservative surgical management. Linear salpingotomy
and segmental resection are now emerging as new
method of management of ectopic pregnancy in order to
preserve the fertility of the patient.

Tubal pregnancy has been thought to implant and grow
within the tubal lumen. But from the present study it appears
that in the tubal implantation the embryo penetrates
into the lamina propria and muscularis to become extraluminal
[8]. The trophoblastic infiltration is predominantly
intraluminal. But extra luminal and mixed pattern
of trophoblastic infiltration was also found in some cases.

Intratubal hemorrhage usually parallel to trophoblastic
spread often leads to marked tubal destruction. The prognosis
of fertility following ectopic pregnancy mainly depends
upon prior history of infertility [9]. Rate of fertility
may be better following salpingostomy than salpingectomy
[10]. It was concluded that early diagnosis and treatment
before rupture still remains the main option of management.